Heart failure (HF) is a debilitating, end-stage disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow may become leaky, allowing regurgitation or backflow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all HF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As HF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output.
Current standard treatment for HF is typically centered around medical treatment using ACE inhibitors, diuretics, and digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Cardiac surgery has also been performed on a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, some HF patients are refractory to drug therapy, have a poor prognosis and limited exercise tolerance. In recent years cardiac pacing has emerged as an effective treatment for many patients with drug-refractory HF.
Notably, magnetic resonance imaging (MRI) scanners produce relatively large radio-frequency (RF) fields during operation. These RF fields may induce a corresponding RF voltage at device lead electrodes across feedthrough capacitors of an implantable cardiac device (ICD) or pacemaker in a patient undergoing MRI scanning. If the RF voltage is sufficiently high, it may result in unintended myocardial stimulation due to a DC current that results from rectification of the induced RF voltage.
This DC rectification current may be particularly large during a fast discharge phase of pacing capacitors for electrodes of the ICD/pacemaker. This is referred to as a cross-channel rectification current, as fast discharge on one channel/electrode generates a DC rectification current on another channel/electrode. The cross-channel rectification current may, for example, cause undesirable atrial fibrillation. Accordingly, it would be desirable to provide patients with an ICD/pacemaker that facilitates preventing unintended myocardial stimulation when subjected to large RF interference.